The objective of this project is to determine the effect of unilateral pulmonary artery occlusion on lung metabolism in an attempt to further define the pathophysiology of human pulmonary thrombo-embolic disease. A better understanding of metabolic changes in the lung may provide important information regarding the biochemical mechanism of pulmonary infarction, and may suggest therapeutic approaches directed at preventing the development of pulmonary infarction. It may also be possible to extrapolate the results of these studies to other clinical disturbances of pulmonary function which may result from alterations in pulmonary arterial perfusion such as the "shock lung", pulmonary fat embolism, and the "pump lung" following cardio-pulmonary by-pass. The model for the study will be the dog with unilateral pulmonary artery ligation. Metabolic studies, using radio-labeled substrates, will be carried out in vitro on lung tissue slices from perfused and non- perfused lung obtained during the first several days following pulmonary artery ligation. Particular emphasis will be directed toward overall energy utilization, as evidenced by tissue oxygen consumption, and the role of glucose and palmitic acid as energy substrates, and as substrates for the synthesis of saturated lecithin, which is an essential component of "surfactant".